The present invention is directed to immunotherapeutic methods for the treatment of benign prostatic hypertrophy.
Benign prostatic hypertrophy (hyperplasia) is a condition involving enlargement of the prostate gland causing variable degrees of bladder outlet obstruction. The condition is commonly seen in men over the age of 50. The etiology of the condition is unknown but may involve alterations in hormonal balance associated with aging. Multiple fibroadenomatous nodules occur in the periurethral region of the prostate gland, probably originating within the periurethral glands themselves rather than in the true fibromuscular prostate, which is displaced peripherally by progressive growth of the hyperplastic nodules. As the lumen of the prostatic urethra is compromised, the outflow of urine is progressively obstructed, with hypertrophy of the bladder detrusor, trabeculation, cellule formation, and diverticula. Incomplete bladder emptying causes stasis and predisposes to infection with secondary inflammatory changes in the bladder and the upper urinary tract. Bladder outlet obstruction symptoms include progressive urinary frequency, urgency, and nocturia due to incomplete emptying and rapid refilling of the bladder. Hesitancy and intermittency with decreased size and force of the urinary stream occur. Sensations of incomplete emptying, terminal dribbling, almost continuous overflow incontinence, or complete urinary retention may ensue.
Therapy for benign prostatic hypertrophy has been surgical with transurethral resection of the prostate (TURP) as the preferred operative procedure. Larger benign prostates may be managed by open surgery using the suprapubic or retropubic approach that permits enucleating of the adenomatous tissue from within the surgical capsule. Nevertheless, there remains a desire in the art for an effective non-surgical treatment for benign pro static hyperplasia.
U.S. Pat. No. 4,002,738 discloses the use of a luteinizing hormone releasing factor (LHRF) sometimes generically known as gonadorelin, which causes luteinizing hormone, a pituitary gonadotropin, to be released from the pituitary to treat various tumors. U.S. Pat. No. 4,321,260 discloses the use of gonadorelin in the treatment of benign prostatic hyperplasia.
McMichael, U.S. Pat. No. 4,692,332 discloses the use of equine chorionic gonadotropin and human chorionic gonadotropin in combination with an immune enhancer such as a lysate of Staphylococcus aureus for treatment of malignant neoplasia. The mechanism of action in the treatment of the cancer was proposed to involve chorionic gonadotropin as a signal molecule capable of inducing apoptosis via membrane changes on the transformed cell at the molecular level, or alternatively by altering the electrical charge of the transformed cell to render it more susceptible to immune elimination. This patent further taught the need to stimulate the cell mediated immune response so that necrotic debris associated with tumor reduction could be efficiently phagocytized to prevent a potentially fatal Herxheimer-type reaction. U.S. Pat. No. 4,692,332, however, fails to disclose the use of chorionic gonadotropin for treatment of non-neoplastic states such as benign prostatic hypertrophy.